Retrograde recanalization of radial artery occlusion via the distal transradial artery: A single-center experience.

Background: Radial artery occlusion (RAO) often occurs after catheterization when using a transradial artery approach. Objective: This prospective study assessed the success and feasibility of accessing the distal transradial artery (dTRA) for retrograde recanalization of RAO. Methods: From June 2019 to December 2021, 44 consecutive patients who had undergone cardiac catheterization resulting in RAO were given retrograde recanalization via the dTRA. According to the result of the procedure (primary endpoint), patients' cases were analyzed as successful or failed. Rates of post-operative patency and adverse events were calculated up to 12 months. Results: The procedural success rate was 88.6%. Compared with the successful group, a significantly higher percentage of patients in the failed group were current smokers and/or suffered from diabetes mellitus (each, 80.0% cf. 33.3%, P = 0.046); had undergone at least 3 previous cardiac catheterizations (60.0% cf. 12.8%, P = 0.011), lower rate of anticoagulation (30.77% cf. 0%, P = 0.048) and exhibited chronic total occlusion (100.0% cf. 51.28%, P = 0.041). In each group, one patient each had minor bleeding at the access site and hematoma. The patency rates in the successful group at postoperative 3, 6, and 12 months were 48.7, 43.6, and 35.9%, respectively. Conclusion: The dTRA approach for retrograde recanalization of RAO showed a high procedural success rate, but with patency rates of <50% at follow-up.

C-Reactive Protein at Hospital Discharge and 1-Year Mortality in Acute Infective Endocarditis: A Prospective Observational Study.

Background: An accurate biomarker at hospital discharge is needed to identify patients with acute infective endocarditis (IE) who are at high risk of mortality. This prospective observational study evaluated the prognostic value of C-reactive protein (CRP). Methods: Patients with acute IE (n = 343) and hospitalized at 2 university-affiliated medical centers from January 2014 to December 2019 were enrolled. Patients were categorized as having low or high CRP (n = 217 and 126, respectively) at hospital discharge according to the optimal cutoff (CRP = 6.5 mg/L) determined via receiver-operating characteristic curve analysis. The primary endpoint was all-cause death, from hospital discharge to 1 year. The secondary endpoint was the cumulative rate of rehospitalization or paravalvular abscess at 1 year. Results: At the 12-month follow-up, the mortality rate of the high-CRP group (21.43%) was significantly higher than that of the low-CRP group (2.76%, log-rank P < 0.0001). The multivariate regression analysis indicated that the high-CRP group had a higher excess mortality hazard risk (HR = 4.182; 95% CI: 2.120, 5.211; P < 0.001). The cumulative 1-year incidence of paravalvular abscess of the high-CRP group (11.90%) was significantly higher than that of the low-CRP (5.07%; P = 0.022). The cumulative rate of heart rehospitalizations of the 2 groups were similar (18.25% cf. 14.29%, P = 0.273). Conclusion: For hospitalized patients with acute IE, a high CRP at discharge suggests a poor prognosis for 1-year mortality and paravalvular abscess.

Accuracy and Prognosis Value of the Sequential Organ Failure Assessment Score Combined With C-Reactive Protein in Patients With Complicated Infective Endocarditis.

This study aimed to evaluate the accuracy and prognostic value of the sequential organ failure assessment (SOFA) score combined with C-reactive protein (CRP) in patients with complicated infective endocarditis (IE). A total of 246 consecutive patients with complicated IE were included in the multicentric prospective observational study. These patients were divided into four groups depending on the SOFA score and CRP optimal cutoff values (≥5 points and ≥17.6 mg/L, respectively), which were determined using the receiver operating characteristic analysis: low SOFA and low CRP (n = 83), low SOFA and high CRP (n = 87), high SOFA and low CRP (n = 25), and high SOFA and high CRP (n = 51). The primary endpoint was in-hospital death, and the secondary endpoint was long-time mortality, defined as subsequent readmission and 3-years mortality in the follow-up period. High SOFA score and high CRP were associated with approximately 29.410% (15/51) of higher incidence of in-hospital death with an area under the curve of 0.872. Multivariate analyses showed that age [odds ratio (OR) = 2.242, 1.142-4.401], neurological failure (Glasgow Coma Scale ≤ 12) (OR = 2.513, 1.041-4.224), Staphylococcus aureus (OR = 2.151, 1.252-4.513), SOFA ≥ 5 (OR = 9.320, 3.621-16.847), and surgical treatment (OR = 0.121, 0.031-0.342) were clinical predictors for in-hospital death. On following up for 12-36 months, SOFA ≥ 5 (p = 0.000) showed higher mortality. A high SOFA score combined with increased CRP levels is associated with in-hospital mortality. Also, SOFA score, but not CRP, predicts long-term mortality in complicated IE.

Satisfactory Long-term Outcomes of Thoracic Endovascular Aortic Repair With a Bare Stent for Acute Complicated Type B Aortic Dissections.

PURPOSE: To compare the clinical outcomes after thoracic endovascular aortic repair (TEVAR) with a bare stent to those after TEVAR alone in patients with complicated acute type B aortic dissection (cATBAD). MATERIALS AND METHODS: A prospective, randomized trial was conducted at 2 medical centers in China between 2010 and 2013. Patients with cATBAD were randomly assigned to receive TEVAR with a bare stent (n=42) or TEVAR only (n=42). Patients were scheduled to undergo computed tomography angiography at 3, 6, and 12 months and then annually to 5 years. The primary endpoint was all-cause mortality at 5 years; secondary outcomes were a composite of complications (endoleak, stent-graft-induced new entry, aortic rupture, and secondary intervention) and aortic remodeling at 1 and 5 years. RESULTS: All-cause death occurred in 1 (2.4%) patient in the TEVAR with bare stent group (lung cancer) and 5 patients (11.9%) in the TEVAR group (4 aorta-related) during the 5-year follow-up (log-rank p=0.025). The 1- and 5-year rates of complications and secondary interventions did not differ between the groups. Patients in the TEVAR with bare stent group had higher increases in the thoracic true lumen diameter (19.7±3.6 vs 17.0±6.2 mm, p=0.018) and abdominal true lumen diameter (13.7±4.8 vs 7.2±6.1 mm, p<0.001) and a higher incidence of complete false lumen thrombosis (80.9% vs 47.6%, p=0.005) at the 1-year follow-up. However, no between-group differences in the changes of aortic remodeling parameters were observed between the 1- and 5-year follow-up periods. CONCLUSION: The addition of a distal bare stent to a thoracic stent-graft during TEVAR was associated with significantly improved long-term survival in cATBAD patients vs TEVAR only, likely due to the prevention of true lumen collapse and improvement of complete false lumen thrombosis of the dissected aorta.

A novel simple experimental model for low-osmolar contrast-induced acute kidney injury using different definitions based on the levels of serum creatinine and cystatin C.

BACKGROUND: It remained lack of a kind of contrast-induced acute kidney injury (CI-AKI) model which was widely used in clinical practice and comparable to CI-AKI in humans. METHODS: Fifty Sprague-Dawley rats were divided into five groups of 10 rats each: (1) sham group (normal saline [NS] + NS); (2) NS plus low osmolality contrast medium (CM15) (NS + CM15); (3) furosemide (FM) plus NS (FM + NS); (4) FM + CM10; and (5) FM + CM15.We measured the levels of serum creatinine (SCr), cystatin C (cys-C) and histopathological scores of kidney tissues. RESULTS: SCr level in the FM + CM15 group were significantly increased after CM exposure compared with baseline levels (32.9 ± 4.57 vs. 158.7 ± 14.48 µmol/L, p < 0.001). Minor changes were found about the SCr levels between the pre- and post-exposure CM or NS treatment in the other groups. Additionally, the cys-C levels after CM exposure were increased compared with pretreatment levels in the FM + CM15 group (0.08 ± 0.03 vs. 0.18 ± 0.05 mg/L, p < 0.001). Minor changes were noted in the FM + NS group before and after NS administration. Only rats in the FM + CM15 group developed CI-AKI with the definitions of SCr or cys-C. Comparing to the FM + NS group, the histopathological scores were significantly increased in the FM + CM15 group. CONCLUSIONS: A simple and reliable animal model for low osmolality contrast medium-induced AKI was established, which is similar to clinical CI-AKI based on different definitions for AKI.

MicroRNA expression profile by next-generation sequencing in a novel rat model of contrast-induced acute kidney injury.

BACKGROUND: MicroRNAs (miRNAs) are known to regulate most biological processes including contrast-induced acute kidney injury (CI-AKI). Few studies have investigated microRNA (miRNAs) expressions in a novel rat model of CI-AKI using nonionic low-osmolar iodic contrast medium Ultravist, and performed gene ontology (GO) categories analysis. METHODS: In this study, kidney tissues were collected from Sprague-Dawley rats at 24 h after contrast-exposure (CI-AKI) and saline-administration (control). MiRNAs microarray assays were used to detect miRNAs in the kidney tissue by next-generation sequencing. Real-time PCR was performed to verify the microarray assays results. All significant differently expressed miRNAs were analyzed by GO categories and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. RESULTS: Of the 173 detected miRNAs, 22 were down-regulated (miR-328a-5p, miR-31a-5p, miR-377-3p, et al.) and 19 were up-regulated (miR-3558-5p, miR-34c-3p, miR-384-5p, et al.) in the kidneys of CI-AKI rats according to log2 (fold change, control) >1, P<0.001 as significant differently expressed miRNAs, which included new differently expressed miRNAs, such as miRNA-1949 and miR-3558. The results showed that a large set of genes involved in essential biological processes were targeted by these miRNAs, such as dysfunction metabolic process, apoptotic process, and endoplasmic reticulum stress, in addition to genes implicated in signaling pathways involved in inflammation and dysfunctional metabolism, including AGE-RAGE signaling pathway and glycerophospholipid metabolism. CONCLUSIONS: The 41 miRNAs identified were differentially expressed in the kidneys of a novel rat model of CI-AKI, and thus possess the potential to serve as novel biological markers and new molecular targets for CI-AKI.

Safe Hydration to Prevent Contrast-Induced Acute Kidney Injury and Worsening Heart Failure in Patients with Renal Insufficiency and Heart Failure Undergoing Coronary Angiography or Percutaneous Coronary Intervention.

An optimal hydration volume (HV) that prevents contrast-induced acute kidney injury (CI-AKI) in patients with renal insufficiency and heart failure (HF) at a high risk of worsening HF (WHF) has not been determined. We aimed to determine a safe HV that prevents CI-AKI and WHF following coronary angiography (CAG) or percutaneous coronary intervention (PCI) in patients with renal insufficiency and HF. We recruited 1,307 patients with renal insufficiency and HF and investigated the relationships between the peri-procedural HV/weight (HV/W) ratio, and the risks of CI-AKI and WHF following CAG or PCI. Higher HV/W quartiles were associated with higher CI-AKI rates (Q1: 6.2%, Q2: 9.1%, Q3: 12.5%, and Q4: 18.7%; P < 0.001) and a greater likelihood of WHF (Q1: 2.2%, Q2: 2.7%, Q3: 4.9%, and Q4: 11.7%; P < 0.001). The multivariate analyses indicated that excessively high HV/W ratios were associated with moderately increased risks of CI-AKI (Q4 versus Q1: adjusted odds ratio [OR] 2.16, 95% confidence interval [CI] 1.17-4.00) and WHF (Q4 versus Q1: adjusted OR 3.09, 95% CI 1.21-7.88). The multivariate Cox regression analysis indicated that a higher HV/W ratio was associated with significantly increased long-term mortality (Q2 versus Q1: adjusted hazard ratio [HR] 2.36; Q3 versus Q1: adjusted HR 2.85; Q4 versus Q1: adjusted HR 2.94; all P < 0.05). In conclusion, an excessively high HV/W might be associated with a moderately increased risk of CI-AKI, WHF, and long-term mortality in patients with renal insufficiency and HF.

Correction: Predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury and mortality following coronary angiography or intervention.

[This corrects the article DOI: 10.18632/oncotarget.19034.].

Association of post-procedural early (within 24h) increases in serum creatinine with all-cause mortality after coronary angiography.

BACKGROUND: The majority of patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI) are discharged early, with only early (within 24h) serum creatinine (SCr) data available without evidence of clinical prognosis. We aimed to systemically evaluate the association between post-procedural early increase in SCr and all-cause mortality following CAG. METHODS: We performed a retrospective sub-study analysis within a prospective observational study including 3091 consecutive patients with baseline and post-procedural early (within 24h) SCr data. The degree (mild, moderate, or large) of absolute and relative increases in SCr from baseline. The mean follow-up time was 2.49years. RESULT: Moderate or large early increases in SCr were relatively rare (large increase: >1.0mg/dl [0.5%], >100% [0.4%]), whereas mild absolute and relative increases in SCr were more common (mild increase: 0.25 to 0.50mg/dl [4.5%], 25% to 50% [5.9%]). During the follow-up period, there were 136 post-procedural deaths (5.6%). After adjustment for confounders, mild absolute and relative increases in SCr were associated with increased mortality (hazard ratio [HR]: 1.9 and 1.8, respectively, both P<0.05). Moderate or large increases in SCr were associated with higher mortality, even higher than with pre-existing renal dysfunction (HR: 5.36 and 4.12 for moderate increase [0.5 to 1.0mg/dl] and estimated glomerular filtration rate<60ml/min). CONCLUSION: Post-procedural mild, moderate, or large early increase in SCr, is associated with significantly increased long-term mortality. Although moderate or large increase in SCr following CAG was relatively rare, the prognosis is more serious, and is worse than that of pre-existing renal dysfunction. CLINICAL TRIAL REGISTRATION: Predictive Value of Contrast Volume to Creatinine Clearance Ratio (PRECOMIN, ClinicalTrials.govNCT01400295).

miR­21 attenuates contrast­induced renal cell apoptosis by targeting PDCD4.

Contrast medium (CM) is widely used in cardiac catheterization; however, it may induce acute kidney injury or renal failure, although the underlying mechanism remains to be elucidated. MicroRNA­21 (miR­21) is involved in renal disease and has been indicated to regulate cellular apoptosis and fibrosis, although its role in CM­induced renal cell injury is unknown. The present study examined the expression and potential targets of miR­21 in human renal proximal tubular epithelial (HK­2) cells following CM treatment. CM induced renal cell apoptosis and decreased miR­21 expression. The expression level of the apoptosis regulator protein, B­cell lymphoma 2 (Bcl­2) was upregulated, whereas that of the apoptosis regulator, Bcl­2­associated X protein (Bax) was downregulated upon transfection of miR­21 mimics; miR­21 overexpression additionally directly inhibited the expression of programmed cell death protein 4 (PDCD4), as determined by a dual luciferase reporter assay, and PDCD4 silencing reduced the rate of HK­2 cell apoptosis. The results of the present study indicated that miR­21 protected renal cells against CM­induced apoptosis by regulating PDCD4 expression.

Association of left ventricular ejection fraction with contrast-induced nephropathy and mortality following coronary angiography or intervention in patients with heart failure.

BACKGROUND: Left ventricular ejection fraction (LVEF) is the most widely used parameter to evaluate the cardiac function in patients with heart failure (HF). However, the association between LVEF and contrast-induced nephropathy (CIN) is still controversial. Therefore, the aim of this study is to evaluate the association of LVEF with CIN and long-term mortality following coronary angiography (CAG) or intervention in patients with HF. METHODS: We analyzed 1,647 patients with HF (New York Heart Association [NYHA] or Killip class >1) undergoing CAG or intervention, including 207 (12.57%) patients with reduced LVEF (HFrEF), 238 (14.45%) with mid-range LVEF (HFmrEF) and 1,202 (72.98%) with preserved LVEF (HFpEF). CIN was defined as an absolute increase of ≥0.5 mg/dL or a relative increase of ≥25% from baseline serum creatinine within 48-72 h after contrast medium exposure. Multivariable logistic regression and Cox proportional hazards regression analyses were performed to identify the association between LVEF, CIN and long-term mortality, respectively. RESULTS: Overall, 225 patients (13.7%) developed CIN. Individuals with lower LVEF were more likely to develop CIN (HFrEF, HFmrEF and HFpEF: 18.4%, 21.8% and 11.2%, respectively; P<0.001), but without a significant trend after adjusting for the confounding factors (HFrEF vs HFpEF: odds ratio [OR] =1.01; HFmrEF vs HFpEF: OR =1.31; all P>0.05). However, advanced HF (NYHA class >2 or Killip class >1) was an independent predictor of CIN (adjusted OR =1.54, 95% confidence interval [CI], 1.07-2.22; P=0.019). During the mean follow-up of 2.3 years, reduced LVEF (HFrEF group) was significantly associated with increased mortality (HFrEF vs HFpEF: adjusted hazard ratio =2.88, 95% CI, 1.77-4.69; P<0.001). CONCLUSION: In patients with HF undergoing CAG or intervention, not worsened LVEF but advanced HF was associated with an increased risk of CIN. In addition, reduced LVEF was an independent predictor of long-term mortality following cardiac catheterization.

Comparing common doses (double-dose vs usual-dose) of atorvastatin for preventing contrast-induced acute kidney injury and mortality after coronary angiography.

High-dose atorvastatin pretreatment was proved reducing the risk of contrast-induced acute kidney injury (CI-AKI), especially in patients with high C-reactive protein (CRP) levels. We evaluated the effects of common atorvastatin doses (double vs usual) on the risk of CI-AKI and mortality.We recorded outcomes from 1319 patients who were administered periprocedural common doses of atorvastatin. The risks of CI-AKI and mortality between double-dose (40 mg/d) and usual-dose atorvastatin (20 mg/d) were compared using multivariable regression models in all patients or CRP tertile subgroups.Seventy-six (5.8%) patients developed CI-AKI. Double-dose atorvastatin compared with usual-dose did not further reduce the risk of CI-AKI (adjusted odds ratio [OR]: 2.28, 95% confidence interval [CI]: 0.92-5.62, P = .074), even for patients in the highest CRP tertile (>8.33 mg/L; adjusted OR: 3.76, 95% CI: 0.83-17.05, P = .086). Similar results were observed in reducing mortality in all patients (adjusted hazard ratio: 0.47, 95% CI: 0.10-2.18; P = .339) and in the highest CRP tertiles (P = .424). In the subgroup analysis, double-dose atorvastatin increased risk of CI-AKI in patients with creatinine clearance (CrCl) < 60 mL/min, anemia, contrast volume > 200 mL and > 2 stents implanted (P = .046, .009, .024, and .026, respectively).Daily periprocedural double-dose atorvastatin was not associated with a reduced risk of CI-AKI compared with usual-dose, and did not provide an improved long-term prognosis, even in patients with high CRP levels. However, it increased the risk of CI-AKI in patients with a high contrast volume/CrCl.

Safe Hydration Volume to Prevent Contrast-induced Acute Kidney Injury and Worsening Heart Failure in Patients With Heart Failure and Preserved Ejection Fraction After Cardiac Catheterization.

Few studies have investigated the efficacy and safety of hydration to prevent contrast-induced acute kidney injury (CI-AKI) and worsening heart failure (WHF) after cardiac catheterization in heart failure and preserved ejection fraction (HFpEF; HF and EF ≥50%) patients. We recruited 1206 patients with HFpEF undergoing cardiac catheterization with periprocedural hydration volume/weight (HV/W) ratio data and investigated the relationship between hydration volumes and risk of CI-AKI and WHF. Incidence of CI-AKI was not significantly reduced in individuals with higher HV/W [quartile (Q) 1, Q2, Q3, and Q4: 9.7%, 10.2%, 12.7%, and 12.2%, respectively; P = 0.219]. Multivariate analysis indicated that higher HV/W ratios were not associated with decreased CI-AKI risks [Q2 vs. Q1: odds ratio (OR), 0.95; Q3 vs. Q1: OR, 1.07; Q4 vs. Q1: OR, 0.92; all P > 0.05]. According to multivariate analysis, higher HV/W significantly increased the WHF risk (Q4 vs. Q1: adjusted OR, 8.13 and 95% confidence interval, 1.03-64.02; P = 0.047). CI-AKI and WHF were associated with a significantly increased risk of long-term mortality (mean follow-up, 2.33 years). For HFpEF patients, an excessively high hydration volume might not be associated with lower risk of CI-AKI but may increase the risk of postprocedure WHF.

Intensity of hydration changes the role of renin-angiotensin-aldosterone system blockers in contrast-induced nephropathy risk after coronary catheterisation in patients with chronic kidney disease.

OBJECTIVE: This study evaluated the potential effect of hydration intensity on the role of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) on contrast-induced nephropathy in patients with renal insufficiency. METHODS: All eligible patients were included and stratified according to hydration intensity defined as saline hydration volume to body weight tertiles: <10.21 mL/kg, 10.21 to <17.86 mL/kg, and ⩾17.86 mL/kg. RESULTS: In total, 84 (6.7%) of 1254 patients developed contrast-induced nephropathy: 6.2% in the ACEI/ARB group versus 10.8% in the non-ACEI/ARB group ( P=0.029), with an adjusted odds ratio (OR) of 0.89 (95% confidence interval (CI) 0.46-1.73, P=0.735). The incidence of contrast-induced nephropathy was lower in the ACEI/ARB group than in the non-ACEI/ARB group in the second tertile ( P=0.031), while not significantly different in the first ( P=0.701) and third ( P=0.254) tertiles. ACEIs/ARBs were independently associated with a lower contrast-induced nephropathy risk (OR 0.26, 95% CI 0.09-0.74, P=0.012) and long-term all-cause death (hazard ratio 0.461, 95% CI 0.282-0.755, P=0.002) only in the second hydration volume to body weight tertile. CONCLUSION: The effects of ACEIs/ARBs on contrast-induced nephropathy risk vary according to saline hydration intensity in chronic kidney disease patients, and may further reduce contrast-induced nephropathy risk in patients administered moderate saline hydration.

Association of lipoprotein(a) with long-term mortality following coronary angiography or percutaneous coronary intervention.

BACKGROUND: There is no consistent evidence to suggest the association of plasma lipoprotein(a) (Lp[a]) with long-term mortality in patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI). HYPOTHESIS: Level of Lp(a) is associated with long-term mortality following CAG or PCI. METHODS: We enrolled 1684 patients with plasma Lp(a) data undergoing CAG or PCI between April 2009 and December 2013. The patients were divided into 2 groups: a low-Lp(a) group (Lp[a] <16.0 mg/dL; n = 842) and a high-Lp(a) group (Lp[a] ≥16.0 mg/dL; n = 842). RESULTS: In-hospital mortality was not significantly different between the high and low Lp(a) groups (0.8% vs 0.5%, respectively; P = 0.364). During the median follow-up period of 1.95 years, the high-Lp(a) group had a higher long-term mortality than did the low-Lp(a) group (5.8% vs 2.5%, respectively; P = 0.003). After adjustment of confounders, multivariate Cox regression analysis revealed that a higher Lp(a) level was an independent predictor of long-term mortality (hazard ratio: 1.96, 95% confidence interval: 1.07-3.59, P = 0.029). CONCLUSIONS: Our data suggested that an elevated Lp(a) level was significantly associated with long-term mortality following CAG or PCI. However, additional larger multicenter studies will be required to investigate the predictive value of Lp(a) levels and evaluate the benefit of controlling Lp(a) levels for patients undergoing CAG or PCI.

Association between prophylactic hydration volume and risk of contrast-induced nephropathy after emergent percutaneous coronary intervention.

BACKGROUND: Intravenous hydration during percutaneous coronary intervention (PCI) significantly reduces the risk of contrast-induced nephropathy (CIN), but there are no well-defined protocols regard¬ing the optimal hydration volume (HV) required to prevent CIN following emergent PCI. Therefore, this study investigates the association between the intravenous HV and CIN after emergent PCI. METHODS: 711 patients were prospectively recruited who had underwent emergent PCI with hydration at routine speed and the relationship was investigated between HV or HV to weight ratio (HV/W) and the CIN risk, which was defined as a ≥ 25% or ≥ 0.5 mg/dL increase in serum creatinine levels from baseline within 48-72 h of exposure to the contrast. RESULTS: The overall CIN incidence was 24.7%. Patients in the higher HV quartiles had elevated CIN rates. Multivariate analysis showed that higher HV/W ratios were not associated with a decreased risk (using the HV) of CIN, but they were associated with an increased risk (using the HV/W) of CIN (Q4 vs. Q1: adjusted odds ratio 1.99; 95% confidence interval 1.05-3.74; p = 0.034). A higher HV/W ratio was not significantly associated with a reduced risk of long-term death (all p > 0.05). CONCLUSIONS: The data suggests that a higher total HV is not associated with a decreased CIN risk or beneficial long-term prognoses, and that excessive HV may increase the risk of CIN after emergent PCI.

Association of N-terminal pro-brain natriuretic peptide with contrast-induced acute kidney injury and long-term mortality in patients with heart failure and mid-range ejection fraction: An observation study.

The potential value of N-terminal pro-brain natriuretic peptide (NT-proBNP) for contrast-induced acute kidney injury (CI-AKI) in patients with heart failure and mid-range ejection fraction (HFmrEF) is unclear. We investigated whether NT-proBNP is associated with CI-AKI and long-term mortality following elective cardiac catheterization in patients with HFmrEF.A total of 174 consecutive patients with HFmrEF undergoing elective coronary angiography or intervention were enrolled. The primary endpoint was the development of CI-AKI, defined as an absolute increase of ≥0.3 mg/dL or ≥ 50% from baseline serum creatinine with 48 hours after contrast medium exposure. Receiver-operating characteristic curve analysis was conducted, and Youden index was used to determine the best cutoff NT-proBNP value. Multivariable logistic regression and Cox proportional hazards regression analyses were performed to identify the independent risk factors for CI-AKI and long-term mortality, respectively.The incidence of CI-AKI was 12.1%. Patients with CI-AKI had higher NT-proBNP values than those without (4373[1561.9-7470.5] vs 1303[625.2-2482.3], P = 0.003). Receiver-operating characteristic curve revealed that NT-proBNP was not significantly different from the Mehran risk score in predicting CI-AKI (area under the curve [AUC] = 0.723 vs 0.767, P = 0.516). The best cutoff NT-proBNP value for CI-AKI was 3299 pg/mL, with 70.6% sensitivity and 83.1% specificity. Multivariable analysis demonstrated that NT-proBNP ≥3299 pg/mL is significantly related to CI-AKI (odds ratio = 12.79; 95% confidence interval, 3.18-51.49; P < 0.001). Cox regression analysis showed that NT-proBNP ≥3299 pg/mL is associated with long-term mortality (adjusted hazard ratio = 11.91; 95%CI, 2.16-65.70; P = 0.004) during follow-up.In patients with HFmrEF, NT-proBNP ≥3299 pg/mL is associated with CI-AKI and long-term mortality following elective coronary angiography or intervention.

Post-Hoc Study: Intravenous Hydration Treatment in Chinese Patients with High Risk of Contrast-Induced Nephropathy Following Percutaneous Coronary Intervention.

Contrast-induced nephropathy (CIN) develops after the injection of iodinated contrast media. This is a post hoc analysis of the data obtained from the TRUST study, which was a prospective, multicentre, observational study conducted to evaluate the safety and tolerability of the contrast medium iopromide in patients undergoing cardiac catheterization from August 2010 to September 2011 in China, conducted to explore the current status, trends and risk predictors of hydration treatment. The status of hydration to prevent CIN in each patient was recorded. Of the total 17,139 patients from the TRUST study (mean age, 60.33 ± 10.38 years), the overall hydration usage was 46.1% in patients undergoing percutaneous coronary intervention (PCI) and 77.4%, 51.7%, and 48.5% in patients with pre-existing renal disease, diabetes mellitus, and hypertension, respectively. The proportion of hydration use increased from 36.5% to 55.5% from August 2010 to September 2011, which was independently associated with risk predictors like older age, pre-existing renal disease, hypertension, diabetes mellitus, prior myocardial infarction, ST segment elevation MI, high contrast dose, multi-vessel disease and reduced LVEF (<45%). Overall, the usage of intravenous hydration treatment for patients with a high risk of CIN following PCI was high in China.

A novel risk score model for prediction of contrast-induced nephropathy after emergent percutaneous coronary intervention.

BACKGROUND: A few studies developed simple risk model for predicting CIN with poor prognosis after emergent PCI. The study aimed to develop and validate a novel tool for predicting the risk of contrast-induced nephropathy (CIN) in patients undergoing emergent percutaneous coronary intervention (PCI). METHODS: 692 consecutive patients undergoing emergent PCI between January 2010 and December 2013 were randomly (2:1) assigned to a development dataset (n=461) and a validation dataset (n=231). Multivariate logistic regression was applied to identify independent predictors of CIN, and established CIN predicting model, whose prognostic accuracy was assessed using the c-statistic for discrimination and the Hosmere Lemeshow test for calibration. RESULTS: The overall incidence of CIN was 55(7.9%). A total of 11 variables were analyzed, including age >75years old, baseline serum creatinine (SCr)>1.5mg/dl, hypotension and the use of intra-aortic balloon pump(IABP), which were identified to enter risk score model (Chen). The incidence of CIN was 32(6.9%) in the development dataset (in low risk (score=0), 1.0%, moderate risk (score:1-2), 13.4%, high risk (score≥3), 90.0%). Compared to the classical Mehran's and ACEF CIN risk score models, the risk score (Chen) across the subgroup of the study population exhibited similar discrimination and predictive ability on CIN (c-statistic:0.828, 0.776, 0.853, respectively), in-hospital mortality, 2, 3-years mortality (c-statistic:0.738.0.750, 0.845, respectively) in the validation population. CONCLUSIONS: Our data showed that this simple risk model exhibited good discrimination and predictive ability on CIN, similar to Mehran's and ACEF score, and even on long-term mortality after emergent PCI.

Predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury and mortality following coronary angiography or intervention.

OBJECTIVE: To investigate the predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury (CI-AKI) and all-cause mortality following coronary angiography or intervention. METHODS: We prospectively investigated 1042 consecutive patients with both baseline and early post-procedural cystatin C measurement undergoing coronary angiography or intervention. CI-AKI was defined as an increase ≥0.3 mg/dL or >50% in serum creatinine from baseline within 48 h post-procedure. Mean follow-up was 2.26 years. RESULTS: Overall, the patients had a CI-AKI incidence was 3.6% (38/1042), mean serum creatinine of 87 µmol/L. Compared with Mehran risk score, post-procedural early absolute increase (AUC: 0.584 vs. 0.706, P = 0.060) and relative increase (AUC: 0.585 vs. 0.706, P = 0.058) in cystatin C had poorer predictive value for CI-AKI. According to multivariate analysis, post-procedural significant early increase (≥0.3 mg/dL or ≥10%) in cystatin C developed in 231 patients (22.2%), was not independent predictor of CI-AKI (adjusted OR: 1.23, 95% CI, 0.56-2.69, P = 0.612), and long-term mortality (adjusted HR: 0.90; P = 0.838). CONCLUSIONS: Our data suggested post-procedural early increase (within 24 h) in cystatin C was not effective for predicting CI-AKI or all-cause mortality following coronary angiography or intervention among patients at relative low risk of CI-AKI, the negative finding of poor predictive value should be further evaluated in larger multicenter trials.